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We show here that HTLV-1-infected T lymphocytes transiently store viral particles as carbohydrate-rich extracellular assemblies that are held together and attached to the cell surface by virally-induced extracellular matrix components, including collagen and agrin, and cellular linker proteins, such as tetherin and galectin-3.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

We recently reported that human T-lymphotropic virus type 1 (HTLV-1) infection is accompanied by a high frequency of CD4(+)FoxP3(+) cells in the circulation.

In asymptomatic carriers of HTLV-1 and in patients with HTLV-1-associated inflammatory and malignant diseases, a high FoxP3(+) cell frequency correlated with inefficient cytotoxic T cell-mediated killing of HTLV-1-infected cells.

In adult T cellleukemia/lymphoma (ATLL), the FoxP3(+) population was distinct from the leukemic T cell clones.

However, the cause of the increase in FoxP3(+) cell frequency in HTLV-1 infection was unknown.

In this study, we report that the plasma concentration of the chemokine CCL22 is abnormally high in HTLV-1-infected subjects and that the concentration is strongly correlated with the frequency of FoxP3(+) cells, which express the CCL22 receptor CCR4.

Further, we show that CCL22 is produced by cells that express the HTLV-1 transactivator protein Tax, and that the increased CCL22 enhances the migration and survival of FoxP3(+) cells in vitro.

Finally, we show that FoxP3(+) cells inhibit the proliferation of ex vivo, autologous leukemic clones from patients with ATLL.

We conclude that HTLV-1-induced CCL22 causes the high frequency of FoxP3(+) cells observed in HTLV-1 infection; these FoxP3(+) cells may both retard the progression of ATLL and HTLV-1-associated inflammatory diseases and contribute to the immune suppression seen in HTLV-1 infection, especially in ATLL.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Adult T cellleukemia/lymphoma (ATL) is a highly aggressive T cell malignancy, and has a poor prognosis.

Recently, allogeneic-hematopoietic stem cell transplantation (allo-HSCT) has been suggested to improve the outcome.

We retrospectively analyzed 15 patients with ATL who had received allo-HSCT in 2 institutions in Hokkaido, Japan.

Calcineurin inhibitor dosage was reduced and administration was discontinued abruptly in 6 of the 15 patients for disease control; as a result, 4 (66.7%) of the 6 patients achieved complete response (CR) or partial response.

Therefore, a graft-versus-leukemia/lymphoma (GVL) effect might be induced by discontinuation of immunosuppression.

Thirteen of the 15 patients were followed up by monitoring HTLV-1 proviral DNA levels.

In 10 of the 11 patients with positive HTLV-1 proviral DNA before allo-HSCT, HTLV-1 proviral DNA became undetectable at least once after allo-HSCT, and only 1 of the 5 patients in whom HTLV-1 proviral DNA became detectable after allo-HSCT relapsed.

Compared to the results of past studies, these results show that allo-HSCT greatly improved the prognosis of ATL and suggest a contribution of the induction of a GVL effect.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

ATL is a fatal malignancy of T lymphocytes caused by HTLV-I infection and remains incurable.

Galectins are a family of animal lectins that function both extracellularly (by interacting with cell surface and extracellular matrix glycoproteins and glycolipids) and intracellularly (by interacting with cytoplasmic and nuclear proteins) to modulate signaling pathways.

We found that protease-resistant galectin-9 by modification of its linker peptide, hG9NC(null), prevented cell growth of HTLV-I-infected T-cell lines and primary ATL cells.

The suppression of cell growth was inhibited by lactose, but not by sucrose, indicating that beta-galactoside binding is essential for hG9NC(null)-induced cell growth suppression. hG9NC(null) induced cell cycle arrest by reducing the expression of cyclin D1, cyclin D2, cyclin B1, Cdk1, Cdk4, Cdk6, Cdc25C and c-Myc, and apoptosis by reducing the expression of XIAP, c-IAP2 and survivin.

Most of these genes are regulated by NF-kappaB, which plays a critical role in oncogenesis by HTLV-I. hG9NC(null) suppressed IkappaBalpha phosphorylation, resulting in suppression of NF-kappaB.

Most importantly, treatment with hG9NC(null) (6.7 mg/kg injected intraperitoneally every day) reduced tumor formation from an HTLV-I-infected T-cell line when these cells were inoculated subcutaneously into SCID mice.

Our results suggest that hG9NC(null) could be a suitable agent for the management of ATL.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Regulatory T (Treg) cells, which represent 5% to 10% of peripheral T cells, regulate the activities of T-cell subsets by performing immunosuppressive functions and thus preventing the development of autoimmune responses.

Recently, it has been demonstrated that the tumor cells in adult T-cellleukemia lymphomas can function as Treg, raising the question of whether any variant of primary cutaneous T-cell lymphoma may also express a regulatory phenotype.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

That HTLV-I infects CD4(+) T cells and enhances their cell growth has been shown as successful long-term in vitro proliferation in the presence of IL-2.

It is known that T cells isolated from HAM patients possess strong ability for cell proliferation in vitro and mRNA of various cytokines are abundantly expressed in CNS tissues of HAM patients.

In this study, we examined the relationship between cell proliferation and ability of in vitro cytokine production of CD4(+) T cell clones isolated from HAM patients.

We started a culture from a single cell to isolate cell clones immediately after drawing blood from the patients using limiting dilution method, which could allow the cell to avoid in vitro HTLV-I infection after initiation of culture.

Many cell clones were obtained and the rate of proliferation efficiency from a single cell was as high as 80%, especially in the 4 weeks' culture cells from HAM patients.

Our results indicate that the ability of cell proliferation in HAM patients is not restricted in HTLV-I-infected T cells.

HTLV-Iuninfected CD4(+) T cells, mainly Th0 cells, also have a strong ability to respond to IL-2-stimulation, showing that unusual immune activation on T cells has been observed in HAM patients.

Recently, it has been shown that allogeneic hematopoietic stem cell transplantation (allo-HSCT) is an effective treatment for ATL, and that HTLV-1 Tax-specific CD8(+) cytotoxic T cells (CTL) contribute to the graft-versus-ATL effect.

In the present study, we, for the first time, analyzed the T-cell receptor (TCR) repertoire of isolated Tax(301-309) (SFHSLHLLF)-specific CTLs in HLA-A*2402(+) ATL patients before and after allo-HSCT by single-cell reverse transcription-PCR.

In addition, a unique conserved amino acid motif of "P-D/P-R" in TCR-beta complementarity-determining region 3 in either BV7- or BV18-expressing CTLs was observed not only in all of the samples from ATL patients, but also in samples from the same patient before and after HSCT.

Furthermore, the P-D/P-R motif-bearing CTL clones established from peripheral blood samples after HSCT exhibited strong killing activity against the HTLV-1-infected T cells of the patient.

Hence, Tax(301-309)-specific CTLs in ATL patients might have a preference for TCR construction and induce strong immune responses against the HTLV-1-infected T cells of patients, which contribute to the graft-versus-ATL effects after allo-HSCT.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Disruption of TCBA1 associated with a de novo t(1;6)(q32.2;q22.3) presenting in a child with developmental delay and recurrent infections.

A boy with developmental delay, particularly of speech, a distinct face, antineutrophil cytoplasmic antibodies, and recurrent infections was found to have an apparently balanced de novo t(1;6)(q32.3;q22.3) translocation.

Fluorescent in situ hybridisation with BAC/PAC clones and long range polymerase chain reaction products assessed in the human genome sequence localised the chromosome 1 breakpoint to a 9.8 kb segment within a hypothetical gene, LOC388735, and the chromosome 6 breakpoint to a 12.8 kb segment in intron 4 of the T-cell lymphoma breakpoint-associated target 1 (TCBA1) gene.

Disruption and/or formation of TCBA1 fusion genes in T cell lymphoma and leukaemia cell lines suggests a role for this gene in tumorigenesis.

HTLV-1 Tax protein plays a critical role in HTLV-1-associated leukemogenesis and is an attractive target for vaccine development.

Although HTLV-1 Tax is the most dominant antigen for HTLV-1-specific CD8(+) CTLs in HTLV-1-infected individuals, few epitopes recognized by CD4(+) helper T lymphocytes in HTLV-1 Tax protein have been described.

The aim of the present study was to study T-helper-cell responses to HTLV-1 Tax and to identify naturally processed MHC class II-restricted epitopes that could be used for vaccine development.

We assessed the ability of the corresponding peptides to elicit helper T-cell responses by in vitro vaccination of purified CD4(+) T lymphocytes.

Both these epitopes were found to be naturally processed by HTLV-1(+) T-cell lymphoma cells and by autologous antigen-presenting cells that were pulsed with HTLV-1 Tax(+) tumor lysates.

Notably, the two newly identified helper T-cell epitopes are found to lie proximal to known CTL epitopes, which will facilitate the development of prophylactic peptide-based vaccine capable of inducing simultaneous CTL and T-helper responses.

CONCLUSION: Our data suggest that HTLV-1 Tax protein could serve as tumor-associated antigen for CD4(+) helper T cells and that the present epitopes might be used for T-cell-based immunotherapy against tumors expressing HTLV-1.

[Publication-country] United States

[Other-IDs] NLM/ NIHMS14245; NLM/ PMC1986724

19. Tözsér J, Weber IT: The protease of human T-cell leukemia virus type-1 is a potential therapeutic target.Curr Pharm Des; 2007;13(12):1285-94[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The protease of human T-cellleukemia virus type-1 is a potential therapeutic target.

Human T-cellleukemia virus type-1 (HTLV-1) is associated with a number of human diseases.

Although the mechanism by which the virus causes diseases is still not known, studies indicate that viral replication is critical for the development of HTLV-1 associated myelopathy, and initial studies suggested that blocking replication with reverse transcriptase inhibitors had a therapeutic effect.

Therefore, based on the success of HIV-1 protease inhibitors, the HTLV-1 protease is also a potential target for chemotherapy.

Furthermore, mutated residues in HIV-1 protease that confer drug resistance are frequently seen in equivalent positions of other retroviral proteases, like HTLV-1 protease.

Therefore, comparison of HTLV-1 and HIV-1 proteases is expected to aid the rational design of broad spectrum inhibitors effective against various retroviral proteases, including the mutant HIV-1 enzymes appearing in drug resistance.

This review describes the characteristics of HTLV-1 protease, makes comparison with HIV-1 protease, and discusses the status of inhibitor development for the HTLV-1 protease.

[Publication-country] Netherlands

[Number-of-references] 45

20. Bitoun E, Davies KE: The robotic mouse: unravelling the function of AF4 in the cerebellum.Cerebellum; 2005;4(4):250-60[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The devastating nature and lack of effective treatments associated with neurodegenerative diseases have stimulated a world-wide search for the elucidation of their molecular basis to which mouse models have made a major contribution.

In combination with transgenic and knockout technologies, large-scale mouse mutagenesis is a powerful approach for the identification of new genes and associated signalling pathways controlling neuronal cell death and survival.

Here we review the characterization of the robotic mouse, a novel model of autosomal dominant cerebellar ataxia isolated from an ENU-mutagenesis programme, which develops adult-onset region-specific Purkinje cell loss and cataracts, and displays defects in early T-cell maturation and general growth retardation.

The mutated protein, Af4, is a member of the AF4/LAF4/FMR2 (ALF) family of putative transcription factors previously implicated in childhood leukaemia and FRAXE mental retardation.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The study evidenced one of the synthetic analogues (11) as a potent cytotoxic and pro-apoptotic agent against several tumor cell lines which also inhibits the TNFalpha-induced NF-kappaB activation in a human leukemiaT cell line.

Human T-cellleukemia/lymphomavirus type 1 (HTLV-1) was the first oncogenic human retrovirus to be discovered, more than 25 years ago.

HTLV-1 infects 15 to 20 million individuals worldwide.

ATLL can be classified into four major subtypes: a smoldering type, a chronic type, a lymphoma type, and a leukemic type.

Because of intrinsic chemoresistance and severe immunosuppression, the survival rate of ATLL patients, especially those who develop the acute leukemic or lymphoma forms, is very poor, and such clonal malignant CD4 expansion remains one of the most severe lymphoproliferations.

[Number-of-references] 63

24. Yoshie O: Expression of CCR4 in adult T-cell leukemia.Leuk Lymphoma; 2005 Feb;46(2):185-90[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

At the cellular level, p13(II) has been found to interfere with cell proliferation and transformation and to promote apoptosis induced by ceramide and Fas ligand.

Assays carried out in T cells (the major targets of HTLV-1 infection in vivo) demonstrate that p13(II)-mediated sensitization to Fas ligand-induced apoptosis can be blocked by an inhibitor of Ras farnesylation, thus implicating Ras signaling as a downstream target of p13(II) function.

The association between five coding ATM alterations in T-ALL, their germline presence, white blood cell count and unfavourable outcome may point to a role for ATM in the development of T-ALL in these children.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Here, we genetically "switched off' the envelope-mediated immunosuppression of an infectious retrovirus, the Friend murine leukemia virus, while preserving mutant envelope infectivity both ex vivo and in vivo, thus allowing us to test the functional importance of envelope-mediated immunosuppression in retrovirus physiology.

Remarkably, we show, in vivo, that the non-IS mutant virus displays the same propagation kinetics as its WT counterpart in irradiated immunocompromised mice but that it is rapidly and totally cleared from normal immunocompetent mice, which become fully protected against a challenge with the WT retrovirus.

In conclusion, our work demonstrates the critical role of Env-induced immunosuppression for retrovirus propagation in vivo and identifies a unique definite target for antiretroviral therapies and vaccine strategies, also characterized in the human T-cellleukemia virus (HTLV) and xenotropic murine leukemia virus-related virus (XMRV) retroviruses, opening unprecedented prospects for the treatment of retroviral diseases.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Only some carriers of humanT celllymphotropic virus type I (HTLV-1) develop adult T cellleukemia/lymphoma (ATLL) after a long latency period, and an association has been reported between chronic refractory eczema, known as infective dermatitis, and young-onset ATLL.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The human T-cellleukemia/lymphomavirus (HTLV) genome, in addition to the structural Gag and Env proteins and retroviral enzymes, carries a region at its 3' end originally designated pX.

To date, we know that this region encodes two essential transcriptional and post-transcriptional positive regulators of viral expression, the Tax and Rex proteins, respectively (reviewed elsewhere in this issue).

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

PURPOSE: To investigate the relationship between serum immunoglobulin levels and corneal opacities in a cohort of patients with human T-celllymphotrophic virus type-1 (HTLV-1).

METHODS: Complete ophthalmologic examination was performed on 44 patients with HTLV-1 infection (25 patients with adult T-cellleukemia/lymphoma [ATL], 18 patients with HTLV-1 that was associated myelopathy/tropical spastic paraparesis [HAM/TSP], and one patient who was asymptomatic).

RESULTS: Corneal opacities were identified in 15 of 25 patients (60%) with ATL and five of 18 patients (28%) with HAM/TSP.

The prevalence of corneal opacities was associated statistically with elevated IgG level (P = .023) in patients with ATL, but not in patients with HAM/TSP (P > .99).

CONCLUSION: Although the mechanism remains unclear, hypergammaglobulinemia is associated with the development of the corneal opacities in patients of African descent with ATL.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Seven isolates of humanT cellleukemia virus type 1 (HTLV-1) were taken in southern India and phylogenetically analyzed to gain new insights into the origin and dissemination of HTLV-1 in the subcontinent.

The new Indian HTLV-1s were found to be members of subgroup A (Transcontinental subgroup) of the Cosmopolitan group.

These results demonstrate that Indian HTLV-1s are genetically heterogeneous and include the most divergent strain of subgroup A.

On the basis of these results, we speculate that subgroup A HTLV- 1s may have been present for thousands of years in India.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] A critical analysis of prognostic factors in North American patients with human T-celllymphotropic virus type-1-associatedadult T-cellleukemia/lymphoma: a multicenter clinicopathologic experience and new prognostic score.

BACKGROUND: To define the clinicopathologic and prognostic features of patients with human T-celllymphotropic virus type-1 (HTLV-1)-associatedadult T-cellleukemia/lymphoma (ATLL) in North America, standard criteria were used to identify patients with ATLL.

The acute subtype predominated (68.5%).

Although the International Prognostic Index and Prognostic Index for peripheral T-cell lymphoma unspecified identified subsets of patients, these models were not completely predictive.

A recursive partitioning analysis was performed on the data, which successfully identified 3 prognostic categories based on Eastern Cooperative Oncology Group performance status, stage, age, and calcium level at diagnosis.

CONCLUSIONS: This series proposed a new prognostic model for patients with HTLV-1-associated ATLL and confirmed a poor outcome for these patients in North America.

Single nucleotide polymorphism (SNP) array-comparative genomic hybridization (CGH), genetic, and expression analyses of the genes mapped within a common breakpoint cluster region in 10p11.2 revealed that in ATLL cells, transcription factor 8 (TCF8) was frequently disrupted by several mechanisms, including mainly epigenetic dysregulation.

TCF8 mutant mice frequently developed invasive CD4(+) T-celllymphomas in the thymus or in ascitic fluid in vivo.

Down-regulation of TCF8 expression in ATLL cells in vitro was associated with resistance to transforming growth factor beta1 (TGF-beta1), a well-known characteristic of ATLL cells, suggesting that escape from TGF-beta1-mediated growth inhibition is important in the pathogenesis of ATLL.

These findings indicate that TCF8 has a tumor suppressor role in ATLL.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Loss of polarity and disruption of cell junctions are common features of epithelial-derived cancer cells, and mounting evidence indicates that such defects have a direct function in the pathology of cancer.

Supporting this idea, results with several different human tumor viruses indicate that their oncogenic potential depends in part on a common ability to inactivate key cell polarity proteins.

For example, adenovirus (Ad) type 9 is unique among human Ads by causing exclusively estrogen-dependent mammary tumors in experimental animals and in having E4 region-encoded open reading frame 1 (E4-ORF1) as its primary oncogenic determinant.

Most notably, the E4-ORF1 PBM mediates interactions with a selected group of cellular PDZ proteins, three of which include the cell polarity proteins Dlg1, PATJ and ZO-2.

Data further indicate that these interactions promote disruption of cell junctions and a loss of cell polarity.

In addition, one or more of the E4-ORF1-interacting cell polarity proteins, as well as the cell polarity protein Scribble, are common targets for the high-risk human papillomavirus (HPV) E6 or human T-cellleukemia virus type 1 (HTLV-1) Tax oncoproteins.

Underscoring the significance of these observations, in humans, high-risk HPV and HTLV-1 are causative agents for cervical cancer and adult T-cellleukemia, respectively.

Consequently, human tumor viruses should serve as powerful tools for deciphering mechanisms whereby disruption of cell junctions and loss of cell polarity contribute to the development of many human cancers.

This review article discusses evidence supporting this hypothesis, with an emphasis on the human Ad E4-ORF1 oncoprotein.

Although CADM1 lacks expression in T lymphocytes of healthy individuals, it is overexpressed in adult T-cellleukemia-lymphoma (ATL) cells.

It has been suggested that the expression of CADM1 protein promotes infiltration of leukemic cells into various organs and tissues, which is one of the frequent clinical manifestations of ATL.

Amino acid sequence alignment revealed that Tiam1 (T-lymphoma invasion and metastasis 1), a Rac-specific guanine nucleotide exchange factor, has a type II PDZ domain similar to those of membrane-associated guanylate kinase homologs (MAGUKs) that are known to bind to the PDZ-BM of CADM1.

In this study, we demonstrated that the cytoplasmic domain of CADM1 directly interacted with the PDZ domain of Tiam1 and induced formation of lamellipodia through Rac activation in HTLV-I-transformed cell lines as well as ATLcell lines.

Our results indicate that Tiam1 integrates signals from CADM1 to regulate the actin cytoskeleton through Rac activation, which may lead to tissue infiltration of leukemic cells in ATL patients.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

More than 40 cases of ATLL treated by allogeneic bone marrow transplantation (BMT) from sibling donors have been reported, while there have been only a few cases of unrelated BMT for treatment of this disease.

We began performing allogeneic BMT from unrelated donors in 1999 to improve the outcome of ATLL patients with no suitable sibling donors.

Eight ATLL patients underwent unrelated BMT; five received the conventional conditioning regimen consisting of cyclophosphamide and total body irradiation, while three received a reduced-intensity preparative regimen.

Two patients died due to encephalopathy of unknown aetiology on days 10 and 35, and one patient died due to progression of ATLL 25 months after BMT.

Five patients are currently alive and disease-free at a median of 20 months after BMT.

Proviral human T-lymphotropic virus type-I (HTLV-I) DNA load in peripheral blood mononuclear cells (PBMCs) was assessed in four cases before and after BMT.

[ISO-abbreviation] Bone Marrow Transplant.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

46. Mesnard JM, Barbeau B, Devaux C: HBZ, a new important player in the mystery of adult T-cell leukemia.Blood; 2006 Dec 15;108(13):3979-82[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] HBZ, a new important player in the mystery of adult T-cellleukemia.

Adult T-cellleukemia (ATL) was first described in 1977.

A link between ATL and human T-cellleukemia virus type 1 (HTLV-1) was clearly established in the early 1980s.

Over the years, many aspects of HTLV-1-induced cellular dysfunctions have been clarified.

Presently, we are still unable to explain the absence of viral Tax protein (thought to play a central role in T-cell transformation) in more than 50% of ATL cells.

A novel HTLV-1 HBZ protein, encoded on the negative strand, was characterized by our group and is currently the subject of intensive research efforts to determine its function in viral replication and/or pathophysiology.

Recently, 4 studies reported on the existence of different HBZ isoforms and have investigated on their function in both ATL cells or animal models.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The ataxia-telangiectasia-mutated (ATM) kinase plays a central role in responses to various forms of DNA damage and has been suggested to facilitate human immunodeficiency virus type 1 (HIV-1) integration.

Notably, ATM overexpression did not stimulate the HIV-1 late gene expression within the context of Rev-independent constructs or the Rex-dependent production of capsid from human T-cellleukemia virus type 1 proviral constructs.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The human T-cellleukemia virus type 1 (HTLV-1) basic leucine zipper factor (HBZ) gene is encoded by the minus strand of the HTLV-1 provirus and transcribed from the 3' long terminal repeat (LTR).

We compared the functions of the proteins derived from the sHBZ and usHBZ transcripts. sHBZ showed a stronger suppression of Tax-mediated transcriptional activation through the 5' LTR than did usHBZ; the level of suppression correlated with the level of protein produced.

The expression of sHBZ had a growth-promoting function in a T-cell line, while usHBZ expression did not.

We thus characterized the sensitivity of ATLL cells to TRAIL in this study.

Although most primary ATLL cells and cell lines expressed TRAIL death receptors on their surface, they showed only restricted sensitivity to TRAIL.

Among the 10 ATLLcell lines examined, one was sensitive, but two had insufficient death-receptor expression, two had an unknown resistant mechanism with abrogation of the death signal upstream of caspase-8, and the remaining five showed attenuation of the signal in both extrinsic and intrinsic pathways by X-linked inhibitor of apoptosis and Bcl-2/Bcl-xL respectively.

Furthermore, the level of HTLV-I tax expression was significantly correlated to TRAIL resistance.

51. Masutani H, Ueda S, Yodoi J: The thioredoxin system in retroviral infection and apoptosis.Cell Death Differ; 2005 Aug;12 Suppl 1:991-8[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Human thioredoxin (TRX) was first identified in human T-cellleukemia virus type I (HTLV-I)-positive T-cell lines and is associated with the pathophysiology of retroviral infections.

Thioredoxin binding protein-2/vitamin D(3) upregulated protein 1 is a growth suppressor and its expression is suppressed in HTLV-I-transformed cells.

Studies of these molecules of the TRX system provide novel insights into the apoptosis associated with retroviral diseases.

Inhibition of NF-kappaB activity reduces cell growth and induces apoptosis of HTLV-I-transformed T cells, suggesting a central role of NF-kappaB in their proliferation and survival.

MATERIALS AND METHODS: Activation status of MyD88 and interleukin (IL)-1R-associated kinase 1 (IRAK1) in HTLV-I-transformed human T cells, MT2, MT4, and HUT102 was examined by using Western blot and immunoprecipitation.

An expression vector encoding a dominant negative MyD88 with a deletion of its death domain (MyD88dn) was transfected into MT2 cells to evaluate roles of MyD88 in spontaneous activation of cytokine gene promoters and transcription factors, proliferation, and apoptosis in HTLV-I-transformed T cells.

RESULTS: Constitutive association of MyD88 with IRAK1 was observed in all three of HTLV-I-transformed T cells, but not in HTLV-I-negative T cells, such as Jurkat, HUT78, and MOLT4.

CONCLUSION: Our results show a novel pathway in NF-kappaB activation in HTLV-I-transformed T cells and further demonstrate a critical role of MyD88 in their dysregulated gene activation, survival, and proliferation.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Phlegmonous gastritis is an acute and severe infectious disease that is occasionally fatal if the diagnosis is delayed.

Alcohol consumption, an immunocompromised state (e.g., due to HIV infection, rheumatoid arthritis, diabetes mellitus, or adult T-cell lymphoma), and mucosal injury of the stomach are reported to be predisposing factors.

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(PMID = 17984755.001).

[ISSN] 0038-4348

[Journal-full-title] Southern medical journal

[ISO-abbreviation] South. Med. J.

[Language] eng

[Publication-type] Case Reports; Letter

[Publication-country] United States

59. Miyagi T, Nagasaki A, Taira T, Shinhama A, Suzuki M, Ohshima K, Takasu N: Extranodal adult T-cell leukemia/lymphoma of the head and neck: a clinicopathological study of nine cases and a review of the literature.Leuk Lymphoma; 2009 Feb;50(2):187-95[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Extranodal adult T-cellleukemia/lymphoma of the head and neck: a clinicopathological study of nine cases and a review of the literature.

Extranodal adult T-cellleukemia/lymphoma (ATLL) of the head and neck is a rare disease.

We studied the clinicopathological features of nine patients with ATLL involving extranodal head and neck sites and conducted a literature review.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

AIM: To investigate the possible relationship between serum levels and avidities of antibodies against tetanus toxoid (TT) and Haemophilus influenzae type b (Hib) in children that were vaccinated after treatment for childhood acute lymphoblastic leukaemia (ALL).

Antibody levels were analysed at three time points: At diagnosis of ALL, after cessation of treatment before vaccination and three weeks after vaccination.

Avidity was measured twice, with a thiocyanate elution assay, at diagnosis of ALL and three weeks after vaccination.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

INTRODUCTION: Mature T/NK celllymphomas (MTNKL) presenting as leukemia are rare and show considerable overlapping of clinical, morphological and immunophenotypic features.

MATERIALS AND METHODS: We reviewed 380 consecutive cases of mature lymphoid neoplasm that presented as leukemia and were diagnosed on morphology and immunophenotyping of bone marrow and/or peripheral blood samples.

It included four cases of T-large granular leukemia (T-LGL), two of T-cell prolymphocytic leukemia small cell variant (T-PLL), two of adult T-cellleukemia/lymphoma (ATLL) and one of primary cutaneous gamma delta T-cell lymphoma (PCGDTCL).

One case of T- PLL small cell variant showed CD4+/CD8- phenotype, while the other revealed CD4-/CD8+ phenotype.

Both cases of ATLL showed CD4+/CD8+/CD25+ phenotype.

TCRalpha/beta was performed in three cases of T-LGL and was positive in all.

CONCLUSION: Mature nodal T/NK cell neoplasms are rare and MTNKL presenting as leukemia are even rarer.

There is an overlap between the immunophenotypic profiles of different MTNKL subtypes and elaborate T/NK cell panels are required for their evaluation.

The aim of present study was to verify the in vitro antitumor activity of a ruthenium complex, cis-(dichloro)tetraammineruthenium(III) chloride (cis-[RuCl(2)(NH(3))(4)]Cl) toward different tumor cell lines.

The cytotoxic activity of a high concentration (2 mg mL(-1)) of cis-[RuCl(2)(NH(3))(4)]Cl toward Jurkat cells correlated with an increased number of annexin V-positive cells and also the presence of DNA fragmentation, suggesting that this compound induces apoptosis in tumor cells.

Thus, a mechanistic understanding of how metal complexes achieve their activities is crucial to their clinical success and to the rational design of new compounds with improved potency.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

HumanT cellleukemia virus type 1 (HTLV-1), the first human retrovirus discovered, is the etiologic agent for a number of disorders; the two most common pathologies include adult T cellleukemia (ATL) and a progressive demyelinating neuroinflammatory disease, HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP).

The neurologic dysfunction associated with HAM/TSP is a result of viral intrusion into the central nervous system (CNS) and the generation of a hyperstimulated host response within the peripheral and central nervous system that includes expanded populations of CD4+ and CD8+ T cells and proinflammatory cytokines/chemokines in the cerebrospinal fluid (CSF).

The mechanisms of neurological degeneration in HAM/TSP have yet to be fully delineated in vivo and may involve the immunogenic properties of the HTLV-1 transactivator protein Tax.

This comprehensive review characterizes the available knowledge to date concerning the effects of HTLV-1 on CNS resident cell populations with emphasis on both viral and host factors contributing to the genesis of HAM/TSP.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

BACKGROUND: Adult T-cellleukemia/lymphoma (ATLL) is an aggressive malignancy which may occur in individuals infected with human T-celllymphotropic virus type-I (HTLV-I).

HTLV-I is endemic in Khorasan, with a frequency of 2.3% in the general population.

As specific cutaneous manifestations of lymphoma may occur in a significant number of patients, we studied these manifestations in ATLL patients admitted to the Hematology and Dermatology Departments of Ghaem Hospital, Mashhad, Iran, during 1995-2004.

METHODS: In this descriptive study, demographic and clinical information was obtained from 23 patients suffering from ATLL with specific cutaneous lesions (atypical lymphocytes on histopathology of cutaneous lesions), and was analyzed statistically.

CONCLUSION: The most common type of specific skin lesion in ATLL was maculopapular eruption, especially with a generalized distribution.